Diabetes Drugs Flashcards

1
Q

Alpha cells

A

glucagon and proglucagon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Beta cells

A

insulin , C-peptide, proinsulin, amylin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Delta cells

A

somatostatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Epsilon cells

A

Ghrelin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Insulin and glucagon are

A

physiological antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Explain urination frequency and osmolarity in Diabetes Mellitus

A

There is increased glucose which means water retention, because water follows salt because the body is trying to dilute and get rid of high blood sugar.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Types of Diabetes Mellitus

A

T1
T2
Gestational
Other conditions of toxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Explain diabetic keto acidosis

A

There is low insulin in the body , which leads to high blood sugar. This leads to frequent urination, dehydration, and loss of electrolytes and hypovolemia. Counter regulatory hormones are released such as glucagon, cortisol, growth hormone and epinephrine, but there is still no insulin.

The body then starts breaking down triglycerides into FFA and glycerol. The glycerol will be used for gluconeogenesis, but it can’t be used because no insulin. The FFA will be metabolized to ketone bodies (B-hydroxybutyate) and also acetone. The ketone bodies will undergo metabolism via the Kreb’s cycle. This process can cause the blood to become acidic and is exacerbated by lower blood volume due to frequent urination causing fluid loss.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Insulin is first synthesized as

A

proinsulin and C-peptide which both have no physiological activity (Two AA chains connected by cysteine bridges)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How is insulin released?

A

Carbs influx the cell, the cells that synthesize insulin get more and more glucose which means more ATP. The increase in ATP results in the inhibition of voltage gated potassium channels. This causes depolarization of the cell membrane which leads to opening of voltage gated calcium channels to allow influx of calcium into the cells . This leads to degranulation and exocytosis of insulin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What happens when insulin is released?

A

It binds to TK receptors which phosphorylates themselves. The phosphorylation leads to the increased number of glucose transporters in the cell membrane. IN Type 1 diabetes, this never happens.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Insulin is a storage hormone. Explain its effect on liver, muscles, and fat tissue.

A

Muscles: increases the synthesis of glucagon which is only for use by the muscles themselves, the glucagon can’t be used to raise glucose levels in the blood stream.

Liver: Increases glycogen synthesis in hepatocytes this is for use in fasting. The stores in the liver will be used to increase glucose levels in the blood stream.

Fat: Insulin will make adipocytes to stop lipolysis and store glucose. Early in the morning a high carb breakfast will stop lipolysis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

The body will give glucose to

A

the brain, muscles, and the excess to fat tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

When exercising . explain importance of strength training

A

You lose fat with strength training because this directs glucose to muscles and less is directed to fat tissue. This prevents storage of too much fat.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

When sugars in the body interact with proteins, this is like frying a steak. Explain this …

A

Glycosylated proteins leads to more AGEs (Advanced glycosylation end products) AGEs leads to more RAGEs which target tissues such as kidneys, heart, retina and can have damaging effects.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Aging effect on immune system

A

Decrease adaptive

Increase innate

17
Q

Rapid acting insulin (pump)

A

Insulin lispro, insulin aspart, insulin glulisine

18
Q

Short-Acting Insulin

A

“Actual insulin” phys ligand ..given in gestational diabetes

19
Q

Intermediate-Acting and Long Acting Insulin

A

Insulin NPH; Insulin Glargine; Insulin Detemir

20
Q

Mixtures of insulins

A

NPL, NPA

21
Q

Before bed insulin

A

Glargine and Detemir

22
Q

Complications associated with insulin

A

Hypoglycemia
Allergic reactions
Lipodystrophy
Increased cancer risk

23
Q

Why does insulin cause weight gain?

A

Insulin is a storing hormone. It enhances fat storage and inhibits lipolysis.

24
Q

What are secretagogues?

A

stimulates the release of patients on insulin( only used in type 2)

25
Q

Secretagogues mechanism

A

target voltage gated potassium channels which leads to depol which leads to calcium influx and insulin degranulation

26
Q

Old class of insulin secretagogues

A
Glimeperide
Glyburide 
Glipizide
Chlorpropamide
Tolbutamide
27
Q

Old class of secretagogues causes (sulfonyureas)

A

weight gain , hematologic toxicity, skin rashes (if patients react to drugs with sulfonyl groups for antibiotic purposes, then they will most certainly react to the old class secretagogues.

28
Q

Newer gen secretogogues

A

Meglitinide analogues –these will cause weigh gain but no rash because no sulfonyl group. Repaglinide and nateglinide.

29
Q

Biguanides (Metformin)

A

Activates AMP=Activated protein kinase (AMPK) this results in the reduction of hepatic glucose.

30
Q

Pioglitazone

A

Targets PPAR-gamma which are TFs which control genes involved in Glucose and Fatty acid metabolism.

Increase glucose transporter expression, decreased free fatty acid level

31
Q

Rosiglitazone

A

Targets PPAR-gamma which are TFs which control genes involved in Glucose and Fatty acid metabolism.

Increase glucose transporter expression, decreased free fatty acid level

32
Q

Acarbose

A

Inhibitor of alpha Glucosidase Reducing Postmeal Glucose Level (Inhibits enzyme from breaking down complex carbs into simple sugars). Increase gas, etc due to build up of carbohydrates.

33
Q

Exenatide

A

Agonist of Glucagon-Like Peptide (GLP-1) receptors and helps insulin do its job. GLP-1 is released in the gut.

GLP-1 is degraded by DPP-4 and if this DDP-4 is inhibited, then it will increase the activity of GLP-1 which results in insulin better doing its job.

34
Q

Line of treatment for T2 DM

A

Diet and exercise
“ + metformin

metformin + another agent

metformin + two other agents

metformin + more complex insulin regimen+ other non-insulin agent.